Attenuation of kinetic properties of 5-HT (serotonin) S2-receptor (3H-Ketanserin) binding sites was detected in tissue homogenate and synaptosomes of cerebral cortex in ischemic edema (Wroblewska et al 1985, 1986). The changes were found at the time of greatest accumulation of tissue water and increased 5-HT release in the brain of gerbils subjected to bilateral carotid artery occlusion for 15 min and 1 hour release. To elucidate further the pathomechanism of cerebral ischemic edema and its association with changes in the 5-HT metabolic pathway we investigated the properties of 5-HT(1A+1B) and 5-HT(1B) receptor binding sites in the same model. Tritiated 5-HT in the presence of cold 5-HT served to detect 5-HT(1A+1B) binding sites while the addition of spiperone permitted the demonstration of 5-HT(1B) binding sites in synaptosomes of cerebral cortex. A significant reduction of 5- HT(1A+1B) and 5-HT(1B) binding sites was seen in the cerebrocortical synaptosomes obtained from brains subjected to ischemia with and without reflow. In addition, the affinity of 3H- 5HT for 5-HT(1B) binding sites was increased as compared to controls. The kinetic changes in 5-HT(1B) binding sites suggest a presynaptic modulation of 5-HT autoreceptors to be present beside an altered function of post-synaptic 5-HT receptors (5- HT(1A+1B) and S2-receptors) in ischemic brain edema.